The Imaging Core was developed in order to support the Mechanisms of Exercise Intolerance in Heart Failure with Preserved Ejection Fraction: `Precision' Therapy Based on Patient Specific Pathophysiology Program Project Grant (PPG) by overseeing the acquisition and analysis of all MR imaging protocols. This will be a shared resource of the entire Program and will play an essential role in developing an efficient, high performing Program. To accomplish this, we have assembled a multidisciplinary team to serve the imaging needs of each project: cardiac (Project 1), skeletal muscle (Project 2), autonomic neurophysiology (Project 3) and pulmonary (Project 4). Based on the needs of the overall Program Project, the Imaging Core has three specific aims: Aim 1. Perform comprehensive cardiac magnetic resonance imaging to define the pathophysiological mechanisms contributing to central limitations of exercise in Heart Failure with Preserved Ejection Fraction (HFpEF). (Project 1). To accomplish Aim 1, patients and controls will undergo an in-depth comprehensive cardiac MRI complete with cardiac stress and contrast-enhancement, in order to assess cardiac morphology, function, perfusion and fibrosis. Aim 2. Perform comprehensive, non-invasive, metabolic assessment of skeletal muscle at rest, during dynamic exercise, and during post-exercise circulatory arrest (Projects 2 and 3). To accomplish Aim 2, patients and controls will perform dynamic lower limb exercise in our state-of-the-art 7T clinical research scanner in order to assess lactate, carnitine and acetylcarnitine dynamics by 1H-magnetic resonance spectroscopy (MRS), and ATP- phosphocreatine (PCr) exchange kinetics by 31P-MRS. Aim 3. Perform quantitative lung water imaging to define the pathophysiological mechanisms contributing to dyspnea on exertion in HFpEF (Project 4). One of the hallmark features of HFpEF is a rapid and pronounced rise in cardiac filling pressures during exercise. This phenomenon increases the capillary hydrostatic pressure and can lead to an accumulation of fluid in the lung interstitium and alveoli; widening the gas exchange barrier. Regional lung water accumulation may therefore represent a principle mechanism driving dyspnea on exertion. We will integrate with Project 4 to test this hypothesis by measuring lung water before and after dynamic exercise. Together, these novel and innovative data will contribute significantly to our mechanistic understanding of exercise intolerance in HFpEF.